Hypertensive emergency

Case: we had one patient presented with epistaxis from left nose and blood pressure of 210/130--------pt had nasal septum surgery 1 week back.....pt dint have any altered consciousness nor pappiloedema...U/a was normal...
Dx: As there is vascular injury but no end organ damage..so he has hypertensive urgency...
Rx: he was give hydralazin...bp came down to 160/100..... was given anterior nasal packing and Abx for nasal packing: ampi+sulbactam....
after 2 days he improved and was discharged...


A sudden rise in blood pressure to >180/120 mm Hg that is associated with end-organ damage is termed a hypertensive emergency

• Accelerated HTN is a sudden, marked elevation in blood pressure associated with end-organ damage but no papilledema (although retinal hemorrhage and exudates are often present).
• Malignant hypertension is a sudden, marked elevation in blood pressure accompanied by end-organ damage including papilledema.
• Hypertensive encephalopathy is a malignant HTN accompanied by cerebral edema, which presents with headache, nausea, vomiting, restlessness, and confusion.
  
  Hypertensive encephalopathy versus stroke: Onset is usually sudden in ischemic or hemorrhagic stroke but insidious in hypertensive encephalopathy..
  
  
  What is the difference between urgency and emergency?
  Urgency denotes severe hypertension (HTN), typically with diastolic blood pressure (DBP) > 130 mmHg, without symptoms or evidence of end-organ damage. The term accelerated hypertension falls in this category, where retinal exudates and hemorrhages are often present.
  Emergency is an acute, life-threatening elevation in BP with evidence of vascular injury + end-organ damage. The term malignant hypertension falls in this category, typified by papilledema.
  
  
  What causes the end-organ damage?Failure of autoregulation to regulate pressure in the arterioles and capillaries with increasing HTN results in disruption of the vascular endothelium. Fibrinoid necrosis results from deposition of plasma elements in the vascular wall, causing narrowing of the vascular lumen. Tissue ischemia as well as leakage of blood and plasma from affected vessels then results, causing end-organ damage.
  
  
  
  What is the treatment for specific hypertensive emergencies?
  

  Goal is the rapid lowering of mean arterial pressure by approximately 20-25% or to a DBP of 100-110 mmHg over 2-6 hours. However, in aortic dissection, the goal is to lower SBP to 100-120 mmHg and MAP below 80 mmHg ASAP, while patients with acute ischemic stroke or hypertensive encephalopathy may require slightly higher BP initially due to cerebral autoregulation.

  
  

  Malignant hypertension with retinal changes and/or hypertensive encephalopathy - Treatment of choice is a rapid, short-acting IV agent, such as nitroprusside (dose: 0.25-0.5 m g/kg/min to a max of 8-10 m g/kg/min; acts within seconds and lasts only a few minutes). Acts as both a veno- and vasodilator. Limited by cyanide or thiocyanate toxicity, especially with prolonged use or in renal insufficiency; do not use for more than 48 hours if possible (antidote is sodium thiosulfate). Other rapid-acting IV agents include labetolol (20mg IV bolus, 0.5-2 mg/min IV gtt), which is both an alpha- and beta-adrenergic blocker; and nicardipine (5-15 mg/hr IV gtt), which is a peripherally-acting calcium-channel antagonist. A newer medication, fenoldopam (0.1-1.6 m g/kg/min IV gtt), which is a pure dopamine agonist, has the advantage increasing renal blood flow and sodium excretion.

  What about hypertensive urgency?
  
  

  The goal is a reduction in blood pressure to 160/110 over several hours with conventional oral therapy. The oral medication used may vary with the clinical scenario - for example, beta-blockers and nitrates would be preferred in patients with coronary disease, while ACE-inhibitors might be useful in patients with a history of diabetes, scleroderma, or congestive heart failure. Loop diuretics are often very helpful initially in asymptomatic patients who are not volume-depleted. Nifedipine is generally not recommended due to rapid hypotension and possible precipitation of ischemic events, while clonidine often causes sedation and dry mouth as well as orthostatic hypotension and may require careful monitoring. There is no proven benefit in the rapid reduction of blood pressure in asymptomatic patients with severe HTN.

  
  

  
  

  check out this link for info: http://intmedweb.wfubmc.edu/blurbs/cards/hypertensive.html